Lots of important information here!! Please read!

It is important that your breeder does genetic testing for HCM.  It is possible to have a negative cattery which means that if all the breeders are negative the kittens will be negative.  IMPORTANT.  Now some breeders will tell you that there is probably more than 2 genes that have been discovered that will produce HCM.  This could be a true statement - what I will tell you is that I have been testing for 10 years and have not had a case of HCM in any of my cats or kittens.  Since I have a genetic guarantee, I would have been told.

Now here are some issues:

Vets have diagnosed DCM as HCM, DCM is Dilated Cardiomyopathy. This is an enlarged heart.  Completely different disease.  HCM can only be determined after death with a necropsy or with a sonogram. Make sure you see a reputable heart doctor.

Next whenever anything goes wrong with your cat, the vet assumes HCM.  Why?  Because 33% of the maine coons have HCM, there are other breeds whose percentages are higher.  If your vet tells you your cat has HCM.  TELL THEM, my breeder genetically tests for HCM and has a negative cattery.  This makes them look for the reason your cat is sick and not assuming that it is "HCM because it is a maine coon".

Here is a scientific explanation for HCM.

Hypertrophic Cardiomyopathy (HCM)

CAUSE: Hypertrophic cardiomyopathy (HCM) is the most commonly diagnosed cardiac disease in cats. Characterized by regional or diffuse thickening of the walls of the ventricle (the primary "pump" muscle of the heart), HCM has been diagnosed in cats as young as 4 months old and as old as 16 years old. Although the definitive cause of feline HCM has not been identified, its prevalence within certain breeds (i.e. Maine Coon cats, Ragdolls) has prompted speculation that at least some forms of HCM are genetic in origin. The finding of mutations in an important cardiac protein called myosin binding protein C in affected lines of Maine Coon and Ragdoll cats supports a heritable, genetic component of HCM in these breeds.

Thickening of the walls of the ventricle is associated with a decreased ventricular chamber volume and abnormal ventricular relaxation (diastolic function) in cats with HCM. Since the amount of blood pumped by the heart per minute (cardiac output) is the product of the amount of blood ejected per contraction (stroke volume) and the heart rate in beats per minute, this decreased chamber volume (and subsequent stroke volume) results in an increased heart rate (tachycardia) as a reflex mechanism to maintain cardiac output and blood pressure. Although this reflex increase in heart rate may maintain normal blood pressure in the short term, it is associated with an increased consumption of oxygen by the heart muscle, to the extent that oxygen demand may exceed supply. This scenario may result in an energy starved heart muscle, with subsequent heart cell death and worsening function. Another consequence of an increased heart rate is that the ventricle has less time to fill between contractions, further diminishing stroke volume and promoting a vicious cycle of reflex tachycardia, decreased time for ventricular filling, and so on. This decreased left ventricular filling also promotes stasis of blood in the left atrium (chamber just before the left ventricle), which ultimately contributes to the development of clinical signs (see below).

CLINICAL SIGNS: Many cats with HCM present without overt signs of illness. In other cases, signs of congestive heart failure including labored or rapid breathing, open-mouth breathing, and lethargy are evident. These signs occur when fluid accumulates in lung tissue (pulmonary edema) or around the lungs (pleural effusion) secondary to elevation of left atrial pressure. A potentially devastating cclud of HCM is thromboembolism. Thromboembolism refers to the development of a clot in the heart (promoted by left atrial enlargement), with ejection of the clot to the systemic circulation. When the clot lodges in the peripheral circulation, it may obstruct blood flow to the region of the heart supplied by the blocked vessel. The site of thromboembolism most commonly observed in cats with HCM is the distal aorta (termed a saddle thrombus), and clinical signs of hind limb paralysis and acute pain in the hind limbs may be observed. Thromboembolism is a poor prognostic indicator in cats with HCM.